Inflammaging and Cardiovascular Disease

Total Page:16

File Type:pdf, Size:1020Kb

Inflammaging and Cardiovascular Disease View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by shahrekord university of medical scinces Phytomedicine 23 (2016) 1119–1126 Contents lists available at ScienceDirect Phytomedicine journal homepage: www.elsevier.com/locate/phymed Inflammaging and cardiovascular disease: Management by medicinal plants ∗ Erfaneh Shayganni a, Mahmoud Bahmani b, Sedigheh Asgary c, Mahmoud Rafieian-Kopaei a, a Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran b Food and Beverages Safety Research Center, Urmia University of Medical Sciences, Urmia, Iran c Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan, Iran a r t i c l e i n f o a b s t r a c t Article history: Background: In aging, a host of molecular and cellular changes occur which accelerate alteration and progres- Received 23 August 2015 sion of inflammatory diseases. These conditions in the elderly people cause appearance of a phenomenon Revised 6 November 2015 which has been denoted as “inflammaging”. Understanding the pathogenesis and finding new methods for Accepted 10 November 2015 management of inflammaging are essential. Purpose: In this paper we tried not only to explain inflammaging and its treatments with concentrating Keywords: on medical plants but to collect a sufficient collection of anti-inflammatory plants with focusing on their Aging mechanism of action. Anti-inflammatory drugs Method: In this review paper, by searching in indexing cites, desired articles were obtained since 1995 by us- Cardiovascular disease ing keywords of inflammation, inflammaging, inflammation pathophysiology, free radicals and inflammation, Inflammation aging inflammation, inflammatory disease, and plants or herbal medicine in inflammation. Inflammaging Medicinal plants Sections: In advanced age the generation of free radicals increases in cardiovascular system. Pathological in- flammation is also associated with production of excess free radicals More importantly, chronic inflammation makes aged people susceptible to age-related diseases. Some medicinal plants have been shown promising results in inhibition of inflammaging. Some other sections such as inflammation and inflammaging in cardio- vascular diseases, oxidative stress in cardiovascular complications, prevention and treatment strategies are presented. Conclusion: The results of published papers show that the symptoms of several inflammatory diseases can be inhibited or treated by active ingredients from medicinal plants. © 2015 Elsevier GmbH. All rights reserved. Introduction ( Nasri and rafieian-kopaei 2013; Rabiei et al. 2013a; Favarato et al. 2014 ). Aging is a phenomenon resulted from genetic, epigenetic The world’s population age is increasing and the aging popula- stochastic, and environmental events in different cells and tissues. tion is a risk factor for cardiovascular diseases (CVD). Aging generally In fact in aging, a host of molecular and cellular changes occur which causes some changes which, even in absence of usual risk factors, ren- accelerate these alterations and implicate in the progression of arte- der the cardiovascular system prone to some diseases ( Lakatta 20 0 0 ). rial diseases ( Rabiei et al. 2013b; Favarato et al. 2014 ). Pathological The progressive degeneration of the heart in elderly makes it inflammation is also associated with production of excess free radi- more vulnerable to stress and causes an increase in cardiovascu- cals arising predominantly from mitochondria ( Beller 2010; Rafieian- lar morbidity and mortality ( Brodsky et al. 2004 ). Cardiovascular kopaei et al. 2012 ). There are also evidences showing that in advanced diseases are also fuelled by some other risk factors such as di- age the generation of free radicals increase in cardiovascular system abetes ( Baradaran et al. 2013; Behradmanesh et al. 2013 ), hyper- ( Judge et al. 2005; Asadbeigi et al. 2014 ). More importantly, chronic tension ( Asgary et al. 2013; Ghorbani et al. 2013 ), and obesity inflammation makes aged people susceptible to age-related diseases ( Franceschi et al. 20 0 0 ). A wide variety of diseases including diabetes ( Asadbeigi et al. Abbreviations: CVD, Cardiovascular diseases; NOS, Nitric oxide synthase; eNOS, En- 2014 ) cancer ( Azadmehr et al. 2011; Nasri and rafieian-kopaei 2014 ), dothelial nitric oxide synthase; LDLox, Oxidized low density lipoprotein; NSAIDs, Non- steroidal anti-inflammatory drugs; DMARDs, Disease-modifying agents of rheumatoid infection (Bagheri 2013; Bagheri 2013), atherosclerosis (Rafieian- diseases; NF-k β, Nuclear factor- kb. Kopaei et al. 2011; Rafieian-Kopaei et al. 2014a ), cardiovascular dis- ∗ Corresponding author. Tel./fax: + 98 383 3330709. eases ( Khosravi-Boroujeni et al., 2013; Sarrafzadegan et al. 2013 ), E-mail address: rafi[email protected] (M. Rafieian-Kopaei). Alzheimer ( Rabiei et al. 2013c, 2014 ) and other degenerative diseases http://dx.doi.org/10.1016/j.phymed.2015.11.004 0944-7113/© 2015 Elsevier GmbH. All rights reserved. 1120 E. Shayganni et al. / Phytomedicine 23 (2016) 1119–1126 ( Mardani et al. 2014; Rafieian-Kopaei et al. 2014b ) are associated with metabolic syndrome are associated with coronary vasculopathy, and increased oxidative stress and inflammatory conditions and are de- with circulating serum factors which mediate the connections be- graded in aging. Moreover, the process of inflammation is involved tween these disease conditions. These circulating mediators are in initiation and development of a wide variety of chronic diseases mostly participated in systemic inflammation. Therefore, these fac- ( Paolisso et al. 1998 ). tors may show the evidence for their connections with cardiovascular In aging the normal balance between the oxidative stress and an- pathology ( Berg and Scherer 2005; Rafieian-Kopaei 2014 ). tioxidant system culminates in cardiovascular complications. These conditions in the elderly people cause appearance of a phenomenon Inflammaging and cardiovascular diseases which has been denoted as “inflammaging”. In fact, the word inflam- maging is used to show inflammatory state in the aged individuals The association between systemic inflammation and increase in ( Franceschi et al. 20 0 0 ). the risk of cardiovascular diseases has stimulated basic and clini- Chronic inflammation in aging tissues “Inflammaging” is a perva- cal investigators to research for precise nature and the differences sive feature of aging and most age-related diseases are associated in the nature of traditional inflammation and inflammaging in rela- with inflammation. In fact inflammaging is described as systemic, tion to cardiovascular diseases. In this regard, although their different low-grade chronic inflammation in aged people, in absence of infec- roles in accelerating atherogenesis remain unresolved, however, it is tion. It is a great risk factor for mortality and morbidity in the elderly known that inflammatory response in elderly is not as fast as younger people ( Zhang et al. 2010 ). individuals. Inflammation can be beneficial facilitating the adapta- A mild inflammation is predictive of, and is associated with many tion, turnover and repair of many tissues. However, this inflammatory aging phenotypes. The etiology of inflammation in aging people and response might be impaired during aging which increase the suscep- its contribution in adverse health events is unknown. The pathways tibility to pathogens ( Griendling and FitzGerald 2003 ). that make us able to control inflammation are not fully established. More importantly, in aging period, a host of molecular and cellu- Hence, understanding the pathogenesis and finding new methods lar changes including genetic, epigenetic and environmental events for management of inflammation are beneficial. This paper, there- occur which increase the progression of arterial diseases. fore, aimed to present the recently published papers regarding in- In aged people, the tissues are mostly in a chronically inflamed flammation in cardiovascular diseases, focusing on the role of oxida- state, with no sign of infection. The generation of free radicals also tive stress. and to summarize the herbal medicines which have had increases, and makes aged people susceptible to cardiovascular dis- promising results in prevention and treatment of this phenomenon. eases ( Asadbeigi et al. 2014 ). Inflammaging is associated with increased levels of IL-1, IL-6, TNF Inflammation and cardiovascular disease and CRP which are independent risk factors for mortality and mor- bidity. In aging process interference occurs with anabolic signaling, Inflammation participates to the pathophysiology of a wide va- IL-6 and tumor necrosis factor-a increase, down-regulating insulin riety of chronic diseases particularly injury and infectious diseases. and insulin-like growth factor-1, as well as erythropoietin signaling Interaction of various cells in the adaptive and innate immune sys- and protein synthesis. Inflammaging can be due to the accumulation tems with inflammatory mediators modulates the acute and chronic of damaged macromolecules and cells which increases with age due inflammation causing various diseases. This coordination in inflam- to increased production and/or inadequate elimination. Inflammag- matory mechanisms triggers remodeling of the extracellular matrix, ing might also be due to increase in harmful agents produced by mi- oxidative stress, tissue injury, angiogenesis and fibrosis in various tis- croorganisms of the human body, including gut microbiota. In aging sues. These inflammatory mechanisms
Recommended publications
  • Brain Inflammaging: Roles of Melatonin, Circadian Clocks
    C al & ellu ic la n r li Im C m Journal of Clinical & Cellular f u o n l o a l n o Hardeland, J Clin Cell Immunol 2018, 9:1 r g u y o J Immunology DOI: 10.4172/2155-9899.1000543 ISSN: 2155-9899 Mini Review Open Access Brain Inflammaging: Roles of Melatonin, Circadian Clocks and Sirtuins Rüdiger Hardeland* Johann Friedrich Blumenbach Institute of Zoology and Anthropology, University of Göttingen, Göttingen, Germany *Corresponding author: Rüdiger Hardeland, Johann Friedrich Blumenbach Institute of Zoology and Anthropology, Bürgerstrasse. 50, D-37073 Göttingen, Germany, Tel: +49-551-395414; E-mail: [email protected] Received date: February 13, 2018; Accepted date: February 26, 2018; Published date: February 28, 2018 Copyright: ©2018 Hardeland R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium. Abstract Inflammaging denotes the contribution of low-grade inflammation to aging and is of particular importance in the brain as it is relevant to development and progression of neurodegeneration and mental disorders resulting thereof. Several processes are involved, such as changes by immunosenescence, release of proinflammatory cytokines by DNA-damaged cells that have developed the senescence-associated secretory phenotype, microglia activation and astrogliosis because of neuronal overexcitation, brain insulin resistance, and increased levels of amyloid-β peptides and oligomers. Melatonin and sirtuin1, which are both part of the circadian oscillator system share neuroprotective and anti-inflammatory properties. In the course of aging, the functioning of the circadian system deteriorates and levels of melatonin and sirtuin1 progressively decline.
    [Show full text]
  • Cellular Senescence: Friend Or Foe to Respiratory Viral Infections?
    Early View Perspective Cellular Senescence: Friend or Foe to Respiratory Viral Infections? William J. Kelley, Rachel L. Zemans, Daniel R. Goldstein Please cite this article as: Kelley WJ, Zemans RL, Goldstein DR. Cellular Senescence: Friend or Foe to Respiratory Viral Infections?. Eur Respir J 2020; in press (https://doi.org/10.1183/13993003.02708-2020). This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Copyright ©ERS 2020. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0. Cellular Senescence: Friend or Foe to Respiratory Viral Infections? William J. Kelley1,2,3 , Rachel L. Zemans1,2 and Daniel R. Goldstein 1,2,3 1:Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA 2:Program in Immunology, University of Michigan, Ann Arbor, MI, USA 3:Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI USA Email of corresponding author: [email protected] Address of corresponding author: NCRC B020-209W 2800 Plymouth Road Ann Arbor, MI 48104, USA Word count: 2750 Take Home Senescence associates with fibrotic lung diseases. Emerging therapies to reduce senescence may treat chronic lung diseases, but the impact of senescence during acute respiratory viral infections is unclear and requires future investigation. Abstract Cellular senescence permanently arrests the replication of various cell types and contributes to age- associated diseases.
    [Show full text]
  • Age-Related Cerebral Small Vessel Disease and Inflammaging
    Li et al. Cell Death and Disease (2020) 11:932 https://doi.org/10.1038/s41419-020-03137-x Cell Death & Disease REVIEW ARTICLE Open Access Age-related cerebral small vessel disease and inflammaging Tiemei Li1,2,YinongHuang1,3,WeiCai1,2, Xiaodong Chen1,2, Xuejiao Men1,2, Tingting Lu1,2, Aiming Wu1,2 and Zhengqi Lu 1,2 Abstract The continued increase in global life expectancy predicts a rising prevalence of age-related cerebral small vessel diseases (CSVD), which requires a better understanding of the underlying molecular mechanisms. In recent years, the concept of “inflammaging” has attracted increasing attention. It refers to the chronic sterile low-grade inflammation in elderly organisms and is involved in the development of a variety of age-related chronic diseases. Inflammaging is a long-term result of chronic physiological stimulation of the immune system, and various cellular and molecular mechanisms (e.g., cellular senescence, immunosenescence, mitochondrial dysfunction, defective autophagy, metaflammation, gut microbiota dysbiosis) are involved. With the deepening understanding of the etiological basis of age-related CSVD, inflammaging is considered to play an important role in its occurrence and development. One of the most critical pathophysiological mechanisms of CSVD is endothelium dysfunction and subsequent blood-brain barrier (BBB) leakage, which gives a clue in the identification of the disease by detecting circulating biological markers of BBB disruption. The regional analysis showed blood markers of vascular inflammation are often associated with deep perforating arteriopathy (DPA), while blood markers of systemic inflammation appear to be associated with cerebral amyloid angiopathy (CAA). Here, we discuss recent findings in the pathophysiology of inflammaging and their effects on the development of age-related CSVD.
    [Show full text]
  • Retinal Inflammaging: Pathogenesis and Prevention
    Vol 4, Issue 4, 2016 ISSN - 2321-4406 Review Article RETINAL INFLAMMAGING: PATHOGENESIS AND PREVENTION ABHA PANDIT1, DEEPTI PANDEY BAHUGUNA2, ABHAY KUMAR PANDEY3*, PANDEY BL4, S Pandit5 1Department of Medicine, Index Medical College Hospital and Research Centre, Indore, Madhya Pradesh, India. 2Consultant, Otorhinolaryngologist, Shri Laxminarayan Marwari Multispeciality Charity Hospital, Varanasi, Uttar Pradesh, India. 3Department of Physiology, Government Medical College, Banda, Uttar Pradesh, India. 4Department of Pharmacology, IMS, Banaras Hindu University, Varanasi, Uttar Pradesh, India. 5Department of Ophthalmology, Health Services, Indore, Madhya Pradesh, India. Email: [email protected] Received: 09 June 2016, Revised and Accepted: 14 June 2016 ABSTRACT Macula lutea, the yellow spot or fovea centralis in eye, serves the distinctive central vision in perceiving visual cues and contributing to task performance. Impaired visual acuity, in later years in life, compromises safety, productivity, and life quality. Carotenoid pigment content declines with cumulation of light-induced damage through aging process in the retina. The progression of resultant macular degeneration is aggravated by oxidative stress, inflammation, raised blood sugar, and vasculopathy associating aging. Senescent dry degeneration involves drusen (a compound of glycolipid and glycol-conjugate core) deposition that impairs metabolic connectivity of upper layers of retina with choroid. Degeneration of retinal pigment epithelium and photoreceptors thus results. The late more severe form of age-related macular degeneration (AMD), involves factors inducing choroidal neovascularization. Leaky neocapillaries speed degenerative process of the retina. Most age-related pathologies are initiated by metabolic disruptions and AMD shares features of systemic atherosclerosis. An aberrant tissue response to free radical stress, vasculopathy, and local ischemic underlies AMD pathogenesis.
    [Show full text]
  • Cellular Senescence and Inflammaging in the Skin Microenvironment
    International Journal of Molecular Sciences Review Cellular Senescence and Inflammaging in the Skin Microenvironment Young In Lee 1,2 , Sooyeon Choi 1, Won Seok Roh 1 , Ju Hee Lee 1,2,* and Tae-Gyun Kim 1,* 1 Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 107-11, Korea; [email protected] (Y.I.L.); [email protected] (S.C.); [email protected] (W.S.R.) 2 Scar Laser and Plastic Surgery Center, Yonsei Cancer Hospital, Yonsei University College of Medicine, Seoul 107-11, Korea * Correspondence: [email protected] (J.H.L.); [email protected] (T.-G.K.); Tel.: +82-2-2228-2080 (J.H.L. & T.-G.K.) Abstract: Cellular senescence and aging result in a reduced ability to manage persistent types of inflammation. Thus, the chronic low-level inflammation associated with aging phenotype is called “inflammaging”. Inflammaging is not only related with age-associated chronic systemic diseases such as cardiovascular disease and diabetes, but also skin aging. As the largest organ of the body, skin is continuously exposed to external stressors such as UV radiation, air particulate matter, and human microbiome. In this review article, we present mechanisms for accumulation of senescence cells in different compartments of the skin based on cell types, and their association with skin resident immune cells to describe changes in cutaneous immunity during the aging process. Keywords: inflammaging; senescence; skin; fibroblasts; keratinocytes; melanocytes; immune cells Citation: Lee, Y.I.; Choi, S.; Roh, W.S.; Lee, J.H.; Kim, T.-G. Cellular Senescence and Inflammaging in the 1.
    [Show full text]
  • Contributions of Age-Related Thymic Involution to Immunosenescence and Inflammaging Rachel Thomas1, Weikan Wang1 and Dong-Ming Su2*
    Thomas et al. Immunity & Ageing (2020) 17:2 https://doi.org/10.1186/s12979-020-0173-8 REVIEW Open Access Contributions of Age-Related Thymic Involution to Immunosenescence and Inflammaging Rachel Thomas1, Weikan Wang1 and Dong-Ming Su2* Abstract Immune system aging is characterized by the paradox of immunosenescence (insufficiency) and inflammaging (over-reaction), which incorporate two sides of the same coin, resulting in immune disorder. Immunosenescence refers to disruption in the structural architecture of immune organs and dysfunction in immune responses, resulting from both aged innate and adaptive immunity. Inflammaging, described as a chronic, sterile, systemic inflammatory condition associated with advanced age, is mainly attributed to somatic cellular senescence-associated secretory phenotype (SASP) and age-related autoimmune predisposition. However, the inability to reduce senescent somatic cells (SSCs), because of immunosenescence, exacerbates inflammaging. Age-related adaptive immune system deviations, particularly altered T cell function, are derived from age-related thymic atrophy or involution, a hallmark of thymic aging. Recently, there have been major developments in understanding how age-related thymic involution contributes to inflammaging and immunosenescence at the cellular and molecular levels, including genetic and epigenetic regulation, as well as developments of many potential rejuvenation strategies. Herein, we discuss the research progress uncovering how age-related thymic involution contributes to immunosenescence and inflammaging, as well as their intersection. We also describe how T cell adaptive immunity mediates inflammaging and plays a crucial role in the progression of age-related neurological and cardiovascular diseases, as well as cancer. We then briefly outline the underlying cellular and molecular mechanisms of age-related thymic involution, and finally summarize potential rejuvenation strategies to restore aged thymic function.
    [Show full text]
  • Reversing the Immune Ageing Clock: Lifestyle Modifications And
    Biogerontology (2018) 19:481–496 https://doi.org/10.1007/s10522-018-9771-7 (0123456789().,-volV)(0123456789().,-volV) REVIEW ARTICLE Reversing the immune ageing clock: lifestyle modifications and pharmacological interventions Niharika A. Duggal Received: 27 June 2018 / Accepted: 16 September 2018 / Published online: 29 September 2018 Ó The Author(s) 2018 Abstract It is widely accepted that ageing is Immune ageing and health accompanied by remodelling of the immune system, including reduced numbers of naı¨ve T cells, increased Over the past 250 years life expectancy has increased senescent or exhausted T cells, compromise to mono- dramatically and is still increasing at 2 years per cyte, neutrophil and natural killer cell function and an decade in most countries. Advancing age is accompa- increase in systemic inflammation. In combination nied by a compromised ability of older adults to these changes result in increased risk of infection, combat bacterial and viral infections (Gavazzi and reduced immune memory, reduced immune tolerance Krause 2002; Molony et al. 2017a, b), increased risk of and immune surveillance, with significant impacts autoimmunity (Goronzy and Weyand 2012), poor upon health in old age. More recently it has become vaccination responses (Del Giudice et al. 2017; Lord clear that the rate of decline in the immune system is 2013) and the re-emergence of latent infections to malleable and can be influenced by environmental produce conditions such as shingles (Schmader 2001). factors such as physical activity as well as pharmaco- All of this contributing towards increased morbidity logical interventions. This review discusses briefly our and mortality in older adults (Pera et al.
    [Show full text]
  • Cellular Senescence and the Senescent Secretory Phenotype: Therapeutic Opportunities
    Cellular senescence and the senescent secretory phenotype: therapeutic opportunities Tamara Tchkonia, … , Judith Campisi, James L. Kirkland J Clin Invest. 2013;123(3):966-972. https://doi.org/10.1172/JCI64098. Review Series Aging is the largest risk factor for most chronic diseases, which account for the majority of morbidity and health care expenditures in developed nations. New findings suggest that aging is a modifiable risk factor, and it may be feasible to delay age-related diseases as a group by modulating fundamental aging mechanisms. One such mechanism is cellular senescence, which can cause chronic inflammation through the senescence-associated secretory phenotype (SASP). We review the mechanisms that induce senescence and the SASP, their associations with chronic disease and frailty, therapeutic opportunities based on targeting senescent cells and the SASP, and potential paths to developing clinical interventions. Find the latest version: https://jci.me/64098/pdf Review series Cellular senescence and the senescent secretory phenotype: therapeutic opportunities Tamara Tchkonia,1 Yi Zhu,1 Jan van Deursen,1 Judith Campisi,2 and James L. Kirkland1 1Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA. 2Buck Institute for Research on Aging, Novato, California, USA. Aging is the largest risk factor for most chronic diseases, which account for the majority of morbidity and health care expenditures in developed nations. New findings suggest that aging is a modifiable risk factor, and it may be feasible to delay age-related diseases as a group by modulating fundamental aging mechanisms. One such mech- anism is cellular senescence, which can cause chronic inflammation through the senescence-associated secretory phenotype (SASP).
    [Show full text]
  • Inflammaging in the Intervertebral Disc
    Article Clinical & Translational Neuroscience January–June 2018: 1–9 ª The Author(s) 2018 Inflammaging in the intervertebral disc Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/2514183X18761146 journals.sagepub.com/home/ctn Aleksandra Sadowska1 , Oliver Nic Hausmann2, and Karin Wuertz-Kozak1,3,4,5 Abstract Degeneration of the intervertebral disc – triggered by ageing, mechanical stress, traumatic injury, infection, inflammation and other factors – has a significant role in the development of low back pain. Back pain not only has a high prevalence, but also a major socio-economic impact. With the ageing population, its occurrence and costs are expected to grow even more in the future. Disc degeneration is characterized by matrix breakdown, loss in proteoglycans and thus water content, disc height loss and an increase in inflammatory molecules. The accumulation of cytokines, such as interleukin (IL)-1 , IL-8 or tumor necrosis factor (TNF)- , together with age-related immune deficiency, leads to the so-called inflammaging – low-grade, chronic inflammation with a crucial role in pain development. Despite the relevance of these molecular processes, current therapies target symptoms, but not underlying causes. This review describes the biological and biomechanical changes that occur in a degenerated disc, discusses the connection between disc degen- eration and inflammaging, highlights factors that enhance the inflammatory processes in disc pathologies and suggests future research avenues. Keywords Intervertebral
    [Show full text]
  • The Role of Cytokines in Extreme Longevity
    Arch. Immunol. Ther. Exp. DOI 10.1007/s00005-015-0377-3 REVIEW Inflammaging and Anti-Inflammaging: The Role of Cytokines in Extreme Longevity 1 2 3 Paola Lucia Minciullo • Antonino Catalano • Giuseppe Mandraffino • 1 2 4 2 Marco Casciaro • Andrea Crucitti • Giuseppe Maltese • Nunziata Morabito • 2 1 2 Antonino Lasco • Sebastiano Gangemi • Giorgio Basile Received: 16 June 2015 / Accepted: 2 November 2015 Ó L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2015 Abstract Longevity and aging are two sides of the same as mediators of cytokines. We believe that if inflammaging is coin, as they both derive from the interaction between a key to understand aging, anti-inflammaging may be one of genetic and environmental factors. Aging is a complex, the secrets of longevity. dynamic biological process characterized by continuous remodeling. One of the most recent theories on aging focuses Keywords Inflammaging Á Anti-inflammaging Á on immune response, and takes into consideration the acti- Cytokine Á Aging Á Longevity vation of subclinical, chronic low-grade inflammation which occurs with aging, named ‘‘inflammaging’’. Long-lived Abbreviations people, especially centenarians, seem to cope with chronic IL Interleukin subclinical inflammation through an anti-inflammatory NK Natural killer cells response, called therefore ‘‘anti-inflammaging’’. In the pre- TNF Tumor necrosis factor sent review, we have focused our attention on the contrast IFN Interferon between inflammaging and anti-inflammaging systems, by IL-18BP IL-18 binding protein evaluating the role of cytokines and their impact on extreme SNPs Single nucleotide polymorphisms longevity. Cytokines are the expression of a network IL-1Ra IL-1 receptor antagonist involving genes, polymorphisms and environment, and are Hsp Heat shock proteins involved both in inflammation and anti-inflammation.
    [Show full text]
  • Deregulation of IL-37 and Its Mirnas Modulators in Sarcopenic Patients
    La Rosa et al. J Transl Med (2021) 19:172 https://doi.org/10.1186/s12967-021-02830-5 Journal of Translational Medicine RESEARCH Open Access Deregulation of IL-37 and its miRNAs modulators in sarcopenic patients after rehabilitation Francesca La Rosa1* , Simone Agostini1, Marina Saresella1, Andrea Saul Costa1, Federica Piancone1, Rossella Miglioli2, Fabio Trecate2 and Mario Clerici1,3 Abstract Background: sarcopenia is a highly prevalent condition in elderly individuals which is characterized by loss of mus- cle mass and functions; recent results showed that it is also associated with infammation. Rehabilitation protocols for sarcopenia are designed to improve physical conditions, but very scarce data are available on their efects on infam- mation We verifed whether in sarcopenic patients the infammation is reduced by rehabilitation and investigated the biological correlates of such efect. Methods: Twenty-one sarcopenic patients undergoing a specifcally-designed rehabilitation program were enrolled in the study. Physical, cognitive and nutritional parameters, as well as the concentration of C-Reactive Protein (CRP), pro-and anti-infammatory cytokines and cytokine production-modulating miRNAs were measured at the beginning (T0) and at end (30-days; T1) of the rehabilitation. Results: Rehabilitation resulted in a signifcant improvement of physical and cognitive conditions; this was accom- panied by a signifcant reduction of CRP (p 0.04) as well as of IL-18 (p 0.008) and IL-37 (p 0.009) concentration. Notably, the concentration of miR-335-3p (p= 0.007) and miR-657, the =two known post-transcriptional= regulators of IL-37 production, was increased by the rehabilitation= protocol. Conclusions: Results herein confrm that successful rehabilitation for sarcopenia results in a reduction of the infam- matory milieu, raise the possibility that IL-37 may be a key target to monitor the rehabilitation-associated improve- ment in sarcopenia, and suggest that this cytokine could be a therapeutic target in sarcopenic patients.
    [Show full text]
  • Ageing Research Reviews Inflammaging As a Common Ground
    Ageing Research Reviews 56 (2019) 100980 Contents lists available at ScienceDirect Ageing Research Reviews journal homepage: www.elsevier.com/locate/arr Review Inflammaging as a common ground for the development and maintenance of sarcopenia, obesity, cardiomyopathy and dysbiosis T Gregory Livshitsa,b,*, Alexander Kalinkovicha a Human Population Biology Research Unit, Department of Anatomy and Anthropology, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv 69978, Israel. b Adelson School of Medicine, Ariel University, Ariel, Israel. ARTICLE INFO ABSTRACT Keywords: Sarcopenia, obesity and their coexistence, obese sarcopenia (OBSP) as well as atherosclerosis-related cardio- Inflammaging vascular diseases (ACVDs), including chronic heart failure (CHF), are among the greatest public health concerns Obesity in the ageing population. A clear age-dependent increased prevalence of sarcopenia and OBSP has been regis- Sarcopenia tered in CHF patients, suggesting mechanistic relationships. Development of OBSP could be mediated by a Atherosclerosis crosstalk between the visceral and subcutaneous adipose tissue (AT) and the skeletal muscle under conditions of Cardiomyopathy low-grade local and systemic inflammation, inflammaging. The present review summarizes the emerging data Dysbiosis supporting the idea that inflammaging may serve as a mutual mechanism governing the development of sar- copenia, OBSP and ACVDs. In support of this hypothesis, various immune cells release pro-inflammatory mediators in the skeletal muscle and myocardium. Subsequently, the endothelial structure is disrupted, and cellular processes, such as mitochondrial activity, mitophagy, and autophagy are impaired. Inflamed myocytes lose their contractile properties, which is characteristic of sarcopenia and CHF. Inflammation may increase the risk of ACVD events in a hyperlipidemia-independent manner. Significant reduction of ACVD event rates, without the lowering of plasma lipids, following a specific targeting of key pro-inflammatory cytokines confirms a key role of inflammation in ACVD pathogenesis.
    [Show full text]